Dyslipidemia is associated with defects in cholesterol metabolism and represents a major risk factor for cardiovascular disease, the most common cause of morbidity and mortality in the US. One common inherited form of dyslipidemia is the metabolic defect in low density lipoproteins (LDL) [familial hypercholesterolemia (FH)] caused by genetic mutations in the LDL receptor (LDLR) gene. MicroRNAs (miRNAs) are small regulatory RNAs that are important in development and progression of disease. It is understood that certain microRNAs have a role cholesterol metabolism. A highly abundant miRNA in the liver, miR-122, which does not directly target LDLR mRNA, regulates cholesterol metabolism by an unknown mechanism. A locked nucleic acid based oligonucleotide inhibitor of miR-122 has been shown to reduce total plasma cholesterol levels in a dose dependent manner (See, e.g., Elmen J, et al. Nature, 2008, 452: 896-900.) However, such oligonucleotide based inhibitors require doses impractical for a therapeutic agent. Furthermore, since the oligonucleotides are administered in finite quantities, repeated administration is required to maintain a long term inhibitory effects, which are necessary for many cholesterol-related disorders, like FH. Notwithstanding the link between miRNAs and cholesterol, and prospects of effective therapeutic agents that treat cholesterol-related disorders by modulating miRNA function, the development of effective and safe approaches for miRNA inhibition in the treatment of cholesterol related disorders has been a significant scientific and therapeutic challenge (See, e.g., Czech, M P. N Engl. J. Med. 354; 11 pg. 1144-1145. (2006).)